An Intimate Relationship

Abstract

We last offered our ideas on the role of reverse EC coupling in the initiation of arrhythmias in 2001.1 At that time we emphasized that spurious Ca2+ release or oscillations in Ca2+ levels could serve as possible triggers for arrhythmias. Since then much has been done to confirm this role for intracellular Ca2+. At that time we did not discuss the role of Ca2+ cycling in the maintenance or conversion of stable tachycardias to VF. However, in consideration of the new data on the role of APD restitution in the initiation of VF (increase in wavebreaks; eg, see Garfinkel et al2), we turn our attention now to the role Ca2+ cycling in the myocyte and its impact on APD restitution relations in the isolated rabbit ventricular cell.3 Goldhaber et al consider the role of Ca2+ using different types of APD restitution protocols to emphasize the dynamic nature of intracellular Ca2+ changes and its subsequent impact on the myocyte APD. In their study APD alternans is coupled to Ca2+ cycling, which in itself is not new since others have observed that APD alternans demonstrates a hystersis and is inhibited with BAPTA-AM buffering.4 Some have suggested that repolarization alternans is more closely associated …